Interpreting Acid–Base Disorders: A Calculator Workflow
Published October 11, 2026 · Last updated October 11, 2026
A step-by-step path through acid–base interpretation: start with the serum anion gap, correct it for albumin, check the delta ratio, verify the expected respiratory compensation, and turn to urine indexes for normal anion gap acidosis.
Acid–base interpretation is best approached as a sequence of small, answerable questions rather than as one large judgment. Each step produces a number — the anion gap, the corrected gap, the delta ratio, an expected compensatory PaCO2 or bicarbonate — and the interpretation comes from comparing each number to the previous step.
The calculators in this workflow cover that arithmetic individually. This guide explains which step each calculator belongs to, what the result is measuring, and how the steps fit together when you interpret an arterial blood gas alongside serum electrolytes.
Start with the serum anion gap
The first branch point is the serum anion gap. It separates a metabolic acidosis into a high anion gap acidosis (HAGMA) from a normal anion gap acidosis (NAGMA), because the size of the gap reflects accumulation of unmeasured anions such as lactate or ketoacids versus loss of bicarbonate. The normal reference range is commonly cited as approximately 8 to 12 mmol/L, though thresholds vary between laboratories.
Use the anion gap calculator to compute the gap from the measured sodium, chloride, and bicarbonate.
Correct the gap for a low albumin
Albumin is the largest unmeasured anion in routine lab testing. When albumin is low, the anion gap is falsely narrowed, and an underlying HAGMA can be hidden. The corrected anion gap calculator applies the Figge adjustment for hypoalbuminemia so that the gap is judged against the patient's actual albumin rather than an assumed value.
Check the delta ratio in a high anion gap acidosis
Once a HAGMA is established, the anion gap delta ratio compares the change in the gap to the change in bicarbonate (ΔAG/ΔHCO3). The ratio is often used to look for a complicating bicarbonate-losing or co-existing alkalosis while the primary gap acidosis is being considered — a single number that tries to summarize whether the acid–base picture is "pure" or mixed.
The formula is (AG − 12) / (24 − HCO3), as used in the anion-gap-delta-ratio calculator.
Verify the respiratory response to a metabolic acidosis
A primary metabolic acidosis should trigger a compensatory respiratory response. Winter's formula calculates the expected arterial PaCO2 from the bicarbonate (expected PaCO2 = 1.5 × HCO3 + 8 ± 2 mmHg). A measured PaCO2 near the expected value indicates an appropriate compensatory response; a value meaningfully outside that window suggests an additional respiratory disorder.
Assess the primary respiratory disorders in the other direction
The workflow also works in reverse. In a primary respiratory acidosis or alkalosis, the respiratory compensation calculator estimates the expected serum bicarbonate for the acute and chronic compensation ranges, and the metabolic alkalosis compensation calculator estimates the expected PaCO2 in metabolic alkalosis (PaCO2 ≈ 40 + 0.6 × (HCO3 − 24)). Comparing the measured value to the expected value helps distinguish an appropriate response from a second, independent disorder.
Use urine indexes when the gap is normal
When the acidosis is a normal anion gap (hyperchloremic) acidosis, the next question is whether the kidney is failing to excrete acid or whether bicarbonate is being lost elsewhere. The urine anion gap, calculated as [urine sodium + urine potassium] − urine chloride, was classically described to help separate renal causes from extrarenal causes such as diarrhea on the basis of urinary acidification.
Calculators in this guide
Related guides
References
- Emmett M, Narins RG. Clinical use of the anion gap. Medicine (Baltimore). 1977;56(1):38-54.
- Kraut JA, Madias NE. Serum anion gap: its uses and limitations in clinical medicine. Clin J Am Soc Nephrol. 2007;2(1):162-174.
- Figge J, et al. Anion gap and hypoalbuminemia. Crit Care Med. 1998;26(11):1807-1810.
- Rastegar A. J Am Soc Nephrol. 2007;18(10):2631-2636.
- Albert MS, Dell RB, Winters RW. Ann Intern Med. 1967;66(2):312-322.
- Rose BD. Clinical Physiology of Acid-Base and Electrolyte Disorders. 5th ed. McGraw-Hill; 2001.
- Battle DC, et al. N Engl J Med. 1988;318(10):594-599.